Endometrial Cancer Treatment–for health professionals (PDQ®)

General Information About Endometrial Cancer

Incidence and Mortality

Estimated new cases and deaths from endometrial (uterine corpus) cancer in the United States in 2015:[1]

New cases: 54,870.

Deaths: 10,170.

Cancer of the endometrium is the most common gynecologic malignancy in the United States and
accounts for 6% of all cancers in women.

Clinical Features

Irregular vaginal bleeding is an early sign, the foremost symptom, and the reason why the majority of patients with the highly curable endometrial tumor are diagnosed with stage I disease.

Risk Factors

Risk factors for the development of endometrial cancer include the following:

Obesity.

Hypertension.

Diabetes mellitus.

Cardiovascular disease is the most common cause of death in patients diagnosed with endometrial cancer because of the early stage of the cancer at diagnosis and the metabolic risk factors.[2]

Diagnostics

To
detect endometrial cancer, a technique that directly samples the endometrial
tissue is mandatory. The Pap smear is not reliable as a screening procedure in
endometrial cancer, although a retrospective study found a strong correlation
between positive cervical cytology and high-risk disease (i.e., high-grade
tumor and deep myometrial invasion) [3] as well as an increased risk of nodal
disease.[4] The degree of tumor differentiation has an important impact on the
natural history of this disease and on treatment selection. An increased
incidence of endometrial cancer has been found in association with prolonged,
unopposed estrogen exposure.[5,6] In contrast, combined estrogen and
progesterone therapy prevents the increase in risk of endometrial cancer
associated with unopposed estrogen use.[7,8] In some patients, an antecedent
history of complex hyperplasia with atypia can be demonstrated. An increased
incidence of endometrial cancer has also been found in association with
tamoxifen treatment of breast cancer (NSABP-B-14), related to the estrogenic effect
of tamoxifen on the endometrium.[9,10] Because of this increase, patients on
tamoxifen should have follow-up pelvic examinations and should be examined if
there is any abnormal uterine bleeding.

Histopathology

The pattern of spread is partially dependent on the degree of cellular
differentiation. Well-differentiated tumors tend to limit their spread to the
surface of the endometrium; myometrial extension is less common. In patients
with poorly differentiated tumors, myometrial invasion occurs much more
frequently. Myometrial invasion is frequently a harbinger of lymph node
involvement and distant metastases and is often independent of the degree of
differentiation.[11,12] Metastatic spread occurs in a characteristic pattern.
Spread to the pelvic and para-aortic nodes is common. When distant metastasis occurs, it most commonly involves the following:

Lungs.

Inguinal and supraclavicular nodes.

Liver.

Bones.

Brain.

Vagina.

Prognostic Factors

Another factor found to correlate with extrauterine and nodal spread of tumor
is involvement of the capillary-lymphatic space on histopathologic
examination.[13] Three prognostic groupings of clinical stage I disease become
possible by careful operative staging. Patients with grade 1 tumors involving
only endometrium and no evidence of intraperitoneal disease (i.e., adnexal
spread) have a low risk (<5%) of nodal involvement.[14]
Patients with grade 2 or 3 tumors and invasion of less than 50% of the
myometrium and no intraperitoneal disease have a 5% to 9% incidence of pelvic
node involvement and a 4% incidence of positive para-aortic nodes. Patients
with deep muscle invasion and high-grade tumors and/or intraperitoneal disease
have a significant risk of nodal spread, 20% to 60% to pelvic nodes and 10% to
30% to para-aortic nodes. One study was directed specifically at stage I,
grade 1 carcinomas of favorable histologic type. The authors identified the following four
statistically significant adverse prognostic factors:[15]

Myometrial invasion.

Vascular invasion.

Eight or more mitoses per ten high-power fields.

An absence
of progesterone receptors.

Another group identified aneuploidy and a high S-phase fraction as predictive
of poor prognosis.[16] A Gynecologic Oncology Group study related
surgical-pathologic parameters and postoperative treatment to recurrence-free
interval and recurrence site. For patients without extrauterine spread, the
greatest determinants of recurrence were grade 3 histology and deep myometrial
invasion. In this study, the frequency of recurrence was greatly increased
with positive pelvic nodes, adnexal metastasis, positive peritoneal cytology,
capillary space involvement, involvement of the isthmus or cervix, and,
particularly, positive para-aortic nodes (includes all grades and depth of
invasion). Of the cases with aortic node metastases, 98% were
in patients with positive pelvic nodes, intra-abdominal metastases, or tumor
invasion of the outer 33% of the myometrium.[17,18]

When the only evidence of extrauterine spread is positive peritoneal cytology,
the influence on outcome is unclear. The value of therapy directed at this
cytologic finding is not well founded.[19-24] As a result, although the collection of cytology specimens is still suggested, a positive result does not upstage the cancer. Other extrauterine disease must be present before
additional postoperative therapy is considered.

One report found progesterone receptor levels to be the single most important
prognostic indicator of 3-year survival in clinical stage I and II disease.
Patients with progesterone receptor levels higher than 100 had a 3-year
disease-free survival of 93% compared with 36% for a level lower than 100. Only
cervical involvement and peritoneal cytology were significant prognostic
variables after adjusting for progesterone receptor levels.[25] Other reports
confirm the importance of hormone receptor status as an independent prognostic
factor.[26] Additionally, immunohistochemical staining of paraffin-embedded
tissue for both estrogen and progesterone receptors has been shown to correlate
with International Federation of Gynecology and Obstetrics grade as well
as survival.[27-29] On the basis of these data, progesterone and estrogen
receptors, assessed either by biochemical or immunohistochemical methods,
should be included, when possible, in the evaluation of stage I and II
patients. The following have also been found to be prognostic indicators of clinical outcome:[29]

Oncogene expression.

DNA ploidy.

The fraction of cells in
S-phase.

For example, overexpression of the Her-2/neu oncogene has been
associated with a poor overall prognosis.[30] A general review of prognostic
factors has been published.[31]

Cellular Classification of Endometrial Cancer

Endometrial cancers are classified in one of the following two categories:

Type 1 may arise from complex atypical hyperplasia and is pathogenetically linked to unopposed estrogenic stimulation.

Type 2 develops from atrophic endometrium and is not linked to hormonally driven pathogenesis.

Characteristic activating oncogenic mutations or amplification and inactivating mutations or deletion of tumor suppressors are seen more in association with one type of mutation versus the other type, but some overlap exists. With the Cancer Genome Atlas and a full genetic display of hundreds of endometrial cancers, four subtypes have been identified that will refine classification and provide prognostic and therapeutic implications.[1]

The most common endometrial cancer cell type is endometrioid adenocarcinoma,
which is composed of malignant glandular epithelial elements; an admixture of
squamous metaplasia is not uncommon. Adenosquamous tumors contain malignant
elements of both glandular and squamous epithelium;[2] clear cell and papillary
serous carcinoma of the endometrium are tumors that are histologically similar
to those noted in the ovary and the fallopian tube, and the prognosis is worse
for these tumors.[3] Mucinous, squamous, and undifferentiated tumors are
rarely encountered. Frequency of endometrial cancer cell types is as follows:

Stage Information for Endometrial Cancer

Definitions: FIGO

The Féderation Internationale de Gynécologie et d’Obstétrique (FIGO) and the American Joint Committee on Cancer (AJCC) have designated staging to define endometrial cancer; the FIGO system is most commonly used.[1,2]

Carcinosarcomas should be staged as carcinoma.[2] FIGO stages are further subdivided by the histologic grade of the tumor, for example, stage IC G2.

Even if it no longer influences staging, retrospective data based on the Surveillance, Epidemiology, and End Results Program suggest that positive peritoneal cytology is an independent risk factor in patients with early-stage endometrial cancer.[3]

Treatment Option Overview

Patients with endometrial cancer who have localized disease are usually curable
by hysterectomy and bilateral salpingo-oophorectomy. Best results are obtained
with either of two standard treatments: hysterectomy or hysterectomy and
adjuvant radiation therapy (when deep invasion of the myometrial muscle [50% of the depth] or grade 3 tumor with myometrial invasion is present). Results
of two randomized trials on the use of external-beam radiation therapy (EBRT) in patients with
stage I disease did not show improved survival but did show reduced locoregional recurrence (3%–4% vs. 12%–14% after 5–6 years' median follow-up, P <.001) with an increase in side effects.[1-3][Level of evidence: 1iiDii] Results of a study by the Danish Endometrial Cancer Group also suggest that the absence of radiation does not improve the survival of patients with stage I, intermediate-risk disease (grade 1 and 2 with >50% myometrial invasion or grade 3 with <50% myometrial invasion).[4]

Vaginal cuff brachytherapy is associated with less radiation-related morbidity than is EBRT and has been shown to be equivalent to EBRT in the adjuvant setting for patients with stage I disease.[5] A subset of patients with stage I disease are at a high risk of recurrence and are eligible for adjuvant therapy. Most patients will do well with surgery alone.

Some patients have regional and distant metastases that,
though occasionally responsive to standard hormone therapy, are rarely
curable. For these patients, standard therapy is inadequate.

Progestational agents have been evaluated as adjuvant therapy in a randomized
clinical trial of stage I disease and have been shown to be of no benefit.
These studies, however, were not stratified according to level of progesterone
receptor in the primary tumor. No trials of adjuvant progestins in more
advanced disease are reported. Determination of progesterone receptors in the
primary tumor is encouraged, and entry onto an appropriate adjuvant trial (if
receptor levels are high) should be considered. If no trial is available, data
from receptors on the primary tumor may help guide therapy for recurrent
disease, should it occur.

Stage I Endometrial Cancer

Uterine serous histologies have higher rates of recurrence than do other stage I endometrioid carcinomas. The outcomes in institutional case series that utilize a policy of adjuvant carboplatin plus paclitaxel, occasionally including radiation therapy, for this histologic subtype, have been published and form the basis of management guidelines.[1-7] The Gynecologic Oncology Group (GOG-0249 [NCT00807768]) trial is comparing this chemotherapy regimen to pelvic radiation.

Standard treatment options:

A total hysterectomy and bilateral salpingo-oophorectomy should be done if the tumor:

Is well or moderately differentiated.

Involves the upper 66% of the corpus.

Has negative peritoneal cytology.

Is without vascular
space invasion.

Has less than a 50% myometrial invasion.

Selected
pelvic lymph nodes may be removed. If they are negative, no postoperative
treatment is indicated. Postoperative treatment with a vaginal cylinder is
advocated by some clinicians.[8]

For all other cases and cell types, a pelvic and selective periaortic node
sampling should be combined with the total hysterectomy and bilateral
salpingo-oophorectomy, if there are no medical or technical contraindications.
One study found that node dissection per se did not significantly add to the
overall morbidity from hysterectomy.[9] While the radiation therapy will reduce the
incidence of local and regional recurrence, improved survival has not been
proven and toxic effects are worse.[10-14] Results
of two randomized trials on the use of adjuvant radiation therapy in patients with
stage I disease did not show improved survival but did show reduced locoregional recurrence (3%–4% vs. 12%–14% after 5–6 years' median follow-up, P <.001) with an increase in side effects.[13,15,16][Level of evidence: 1iiDii]
Results of a study by the Danish Endometrial Cancer Group also suggest that the absence of radiation does not improve the survival of patients with stage I, intermediate-risk disease (grade 1 and 2 with >50% myometrial invasion or grade 3 with <50% myometrial invasion).[17]

The PORTEC-2 (NCT00411138) trial randomly assigned patients with stage I endometrial cancer who did not undergo lymph node dissection to undergo vaginal brachytherapy (VBT) or external-beam radiation therapy (EBRT), with prevention of vaginal recurrence as the primary outcome.[18] At 5 years, there was no difference in the rates of vaginal recurrence, locoregional recurrence, progression-free survival or overall survival (OS) (84.8% [95% confidence interval (CI), 79.3–90.3] vs. 79.6% [95% CI, 71.2–88.0] for VBT and EBRT, respectively; P = .57). There were significantly fewer gastrointestinal toxic effects and significantly improved quality of life in the VBT group, making VBT the preferred option for adjuvant treatment of patients with stage I disease.[18,19][Level of evidence: 1iA]

Patients who have medical
contraindications to surgery may be treated with radiation therapy alone,
but inferior cure rates below those attained with surgery may occur.[8,20,21]

Several randomized trials have compared total laparoscopic hysterectomy (TLH) with the standard open procedure, total abdominal hysterectomy (TAH), for patients with early-stage endometrial cancer. Feasibility of the laparoscopic approach has been confirmed, although TLH is associated with a longer operative time.[22-24] TLH had an improved [22,23] or similar [24] adverse event profile and a shorter hospital stay [22-24] when compared with TAH. TLH was associated with less pain and quicker resumption of daily activities,[24,25] although one study found that most of the gains in quality of life favoring laparoscopy at the 6-week postsurgical period were no longer significant at 6 months.[24,25]

The completed GOG-Lamina-associated polypeptide 2 (GOG-LAP2) trial included 2,616 patients with clinical stage I to IIA disease and randomly assigned them two-to-one to comprehensive surgical staging via laparoscopy or laparotomy.[26] Time to recurrence was the primary endpoint, with noninferiority defined as a difference in recurrence rate of less than 5.3% between the two groups at 3 years. The recurrence rate at 3 years was 10.24% for patients in the laparotomy arm, compared with 11.39% for patients in the laparoscopy arm, with an estimated difference between groups of 1.14% (90% lower bound, -1.278; 95% upper bound, 3.996). Although this difference was lower than the prespecified limit, the statistical requirements for noninferiority were not met because of a lower-than-expected number of recurrences in both groups. A Cochrane Review of the use of laparoscopic staging included four randomized controlled trials that reported OS and PFS, although 90% of the patients were from the GOG-LAP2 trial. Overall, laparoscopy was associated with similar OS and PFS rates when it was compared with laparotomy.[27][Level of evidence: 1iiA]The OS at 5 years was 89.8% in both groups. Future analyses may determine whether there are subgroups of patients for whom there is a clinically significant decrement when laparoscopic staging is utilized.[26][Level of evidence: 1iiDiii]

Current Clinical Trials

Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with
stage I endometrial carcinoma. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.

General information about clinical trials is also available from the NCI Web site.

Stage II Endometrial Cancer

Uterine serous histologies have higher rates of recurrence than do other stage II endometrioid carcinomas. The outcomes in institutional case series that utilize a policy of adjuvant carboplatin plus paclitaxel, occasionally including radiation therapy, for this histologic subtype have been published and form the basis of management guidelines.[1,2] The GOG-0249 (NCT00807768) trial is comparing this chemotherapy regimen to pelvic radiation.

If the cervix is clinically uninvolved but extension to the cervix is documented on postoperative pathology, radiation therapy should be considered.

The completed GOG-LAP2 trial included 2,616 patients with clinical stage I to IIA disease and randomly assigned them two-to-one to comprehensive surgical staging via laparoscopy or laparotomy.[3] Time to recurrence was the primary endpoint, with noninferiority defined as a difference in recurrence rate of less than 5.3% between the two groups at 3 years. The recurrence rate at 3 years was 10.24% for patients in the laparotomy arm, compared with 11.39% for patients in the laparoscopy arm, with an estimated difference between groups of 1.14% (90% lower bound, -1.278; 95% upper bound, 3.996). Although this difference was lower than the prespecified limit, the statistical requirements for noninferiority were not met because of a lower-than-expected number of recurrences in both groups. The OS at 5 years was 89.8% in both groups. Future analyses may determine whether there are subgroups of patients for whom there is a clinically significant decrement when laparoscopic staging is utilized.[3][Level of evidence: 1iiDiii]

Current Clinical Trials

Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with
stage II endometrial carcinoma. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.

General information about clinical trials is also available from the NCI Web site.

Stage III Endometrial Cancer

Standard treatment options:

In general, patients with stage III endometrial cancer are treated with surgery, followed by chemotherapy, or radiation therapy, or both.
For many years, radiation therapy was the standard adjuvant treatment for patients with endometrial cancer. However, several randomized trials have confirmed improved survival when adjuvant chemotherapy is used instead of radiation therapy. In a trial conducted in a subset of patients with stage III or IV disease with residual tumors smaller than 2 cm and no parenchymal organ involvement, the use of the combination of cisplatin and doxorubicin resulted in improved overall survival (OS) compared with whole-abdominal radiation therapy (adjusted hazard ratio, 0.68; 95% confidence interval limits, 0.52–0.89; P = .02; 5-year survival rates of 55% vs. 42%).[1][Level of evidence: 1iiA]

In a subsequent trial, paclitaxel with doxorubicin had an outcome similar to that of cisplatin with doxorubicin.[2,3] The three-drug regimen (doxorubicin, cisplatin, and paclitaxel) with granulocyte colony-stimulating factor (G-CSF), however, was significantly superior to cisplatin plus doxorubicin: response rates were 57% versus 34%; progression-free survival was 8.3 months versus 5.3 months; and OS was 15.3 months versus 12.3 months, respectively. The superior regimen was associated with a 12% grade 3 and a 27% grade 2 peripheral neuropathy.[2,3][Level of evidence: 1iiDiv]

Given the toxicity and limited efficacy of these regimens, other treatment options have been widely sought. Several observational studies [4,5] and phase II studies [6-9] suggested clinical activity with the combination of platinums and paclitaxel in endometrial cancer patients with measurable disease either following primary surgery or at recurrence. As a result, the Gynecologic Oncology Group (GOG) opened protocol GOG-0209 (NCT000063999), a noninferiority trial that compared the combination of doxorubicin, cisplatin, and paclitaxel (TAP) with G-CSF to carboplatin and paclitaxel. The interim results, currently available in abstract form, showing that carboplatin and paclitaxel is not inferior to TAP have lent credence to the use of carboplatin and paclitaxel as the standard for adjuvant treatment of stage III and IV disease.

Patients with inoperable disease caused by tumor that extends to the pelvic wall may be treated with a combination of chemotherapy and radiation therapy. The usual
approach is to use a combination of intracavitary radiation therapy and external-beam radiation
therapy.

Patients who are not candidates for either surgery or radiation therapy may
be treated with progestational agents. Studies of patterns of failure have found a high rate of distant
metastases in the upper abdominal and extra-abdominal sites. For this reason,
patients with stage III disease may be candidates for innovative clinical
trials.[10]

Treatment options under clinical evaluation:

The use of biological agents alone, or in combination with chemotherapy, is being investigated in multiple clinical trials.

Current Clinical Trials

Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with
stage III endometrial carcinoma. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.

General information about clinical trials is also available from the NCI Web site.

Stage IV Endometrial Cancer

Treatment of patients with stage IV endometrial cancer is dictated by the site of metastatic
disease and symptoms related to disease sites. For bulky pelvic disease,
radiation therapy consisting of a combination of intracavitary and external-beam radiation therapy is used. When distant metastases, especially pulmonary
metastases, are present, hormonal therapy is indicated and useful.
Observational studies support maximal cytoreductive surgery for patients with stage IV disease, although these conclusions need to be interpreted with care because of the small number of cases and likely selection bias.

When possible, patients with stage IV endometrial cancer are treated with surgery, followed by chemotherapy, or radiation therapy, or both. For many years, radiation therapy was the standard adjuvant treatment for patients with endometrial cancer. However, several randomized trials have confirmed improved survival when adjuvant chemotherapy is used instead of radiation therapy. In a trial conducted in a subset of patients with stage III or IV disease with residual tumors smaller than 2 cm and no parenchymal organ involvement, the use of the combination of cisplatin and doxorubicin resulted in improved overall survival (OS) compared with whole-abdominal radiation therapy (adjusted hazard ratio, 0.68; 95% confidence interval limits, 0.52–0.89; P = .02; 5-year survival rates of 55% vs. 42%).[1][Level of evidence: 1iiA]

In a subsequent trial, paclitaxel with doxorubicin had an outcome similar to that of cisplatin with doxorubicin.[2,3] The three-drug regimen (doxorubicin, cisplatin, and paclitaxel) with granulocyte colony-stimulating factor (G-CSF), however, was significantly superior to cisplatin plus doxorubicin: response rates were 57% versus 34%; progression-free survival was 8.3 months versus 5.3 months; and OS was 15.3 months versus 12.3 months, respectively. The superior regimen was associated with a 12% grade 3 and a 27% grade 2 peripheral neuropathy.[2,3][Level of evidence: 1iiDiv]

Given the toxicity and limited efficacy of these regimens, other treatment options have been widely sought. Several observational studies [4,5] and phase II studies [6-9] suggested clinical activity with the combination of platinums and paclitaxel in endometrial cancer patients with measurable disease either following primary surgery or at recurrence. As a result, the Gynecologic Oncology Group (GOG) opened protocol GOG-0209 (NCT000063999), a noninferiority trial that compared the combination of doxorubicin, cisplatin, and paclitaxel (TAP) and G-CSF with carboplatin and paclitaxel. The interim results, currently available in abstract form, showing that carboplatin and paclitaxel is not inferior to TAP have lent credence to the use of carboplatin and paclitaxel as the standard for adjuvant treatment in stage III and IV disease.

The most common hormonal treatment has been progestational agents, which
produce good antitumor responses in as many as 15% to 30% of patients. These
responses are associated with significant improvement in survival.
Progesterone and estrogen hormone receptors have been identified in
endometrial carcinoma tissues. Responses to hormones are correlated with the
presence and level of hormone receptors and the degree of tumor
differentiation. Standard progestational agents include hydroxyprogesterone, medroxyprogesterone, and megestrol.[10]

Biologic agents under evaluation for patients with advanced and recurrent endometrial cancer include:

Bevacizumab, which was given as a single agent in a phase II trial, and the overall response rate was 13.5%.[11]

All patients with advanced disease should be considered for clinical trials
that evaluate single-agent or combination therapy for this disease.

Current Clinical Trials

Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with
stage IV endometrial carcinoma. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.

General information about clinical trials is also available from the NCI Web site.

Recurrent Endometrial Cancer

For patients with localized recurrences (pelvis and periaortic lymph nodes) or distant
metastases in selected sites, radiation therapy may be an effective palliative
therapy. In rare instances, pelvic radiation therapy may be curative in pure vaginal
recurrence when no prior radiation therapy has been used. Patients positive for
estrogen and progesterone receptors respond best to progestin therapy. Among
115 patients with advanced endometrial cancer who were treated with progestins,
75% (42 of 56 patients) of those with detectable progesterone receptors in their tumors
before treatment responded, compared with only 7% without detectable progesterone
receptors (4 of 59 patients).[1] A receptor-poor status may predict not only poor
response to progestins but also a better response to cytotoxic
chemotherapy.[2] Evidence suggests that tamoxifen (20 mg
twice a day) will give a response rate of 20% in those who do not respond to
standard progesterone therapy.[3]

Several randomized trials by the Gynecologic Oncology Group have utilized the known antitumor activity of doxorubicin. The addition of cisplatin to doxorubicin increased response rates and progression-free survival (PFS) over doxorubicin alone but without an effect on overall survival (OS).[4] However, in a trial conducted in a subset of patients with stage III or IV disease with residual tumors smaller than 2 cm and no parenchymal organ involvement, the use of the combination of cisplatin and doxorubicin resulted in improved OS compared with whole-abdominal radiation therapy (adjusted hazard ratio, 0.68; 95% confidence interval limits, 0.52–0.89; P = .02; 5-year survival rate of 55% vs. 42%).[5][Level of evidence: 1iiA] In a subsequent trial, paclitaxel with doxorubicin had a similar outcome to cisplatin with doxorubicin.[6,7] The three-drug regimen (doxorubicin, cisplatin, and paclitaxel) with granulocyte colony-stimulating factor, however, was significantly superior to cisplatin plus doxorubicin: response rates were 57% versus 34%, PFS was 8.3 months versus 5.3 months, and OS was 15.3 months versus 12.3 months, respectively. The superior regimen was associated with a 12% grade 3 and a 27% grade 2 peripheral neuropathy.[6,7][Level of evidence: 1iiDiv]

Biologic agents under evaluation for patients with advanced and recurrent endometrial cancer include:

Bevacizumab, which was given as a single agent in a phase II trial, and the overall response rate was 13.5%.[8]

Clinical trials are appropriate for patients
whose disease recurs with distant metastases and who are unresponsive to
hormonal therapy.[10] Doxorubicin is the most active anticancer agent employed,
with useful but temporary responses obtained in as many as 33% of patients
with metastatic disease. Paclitaxel, in combination with platinums or as a single agent, also has significant activity.[11]

Current Clinical Trials

Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with
recurrent endometrial carcinoma. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.

General information about clinical trials is also available from the NCI Web site.

About This PDQ Summary

Purpose of This Summary

This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the treatment of endometrial cancer. It is intended as a resource to inform and assist clinicians who care for cancer patients. It does not provide formal guidelines or recommendations for making health care decisions.

Reviewers and Updates

This summary is reviewed regularly and updated as necessary by the PDQ Adult Treatment Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).

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be cited with text, or

replace or update an existing article that is already cited.

Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.

The lead reviewers for Endometrial Cancer Treatment are:

Leslie R. Boyd, MD (New York University Medical Center)

Franco M. Muggia, MD (New York University Medical Center)

Any comments or questions about the summary content should be submitted to Cancer.gov through the Web site's Contact Form. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.

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Updated: April
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